U P D AT E O N

AC U T E C O RO NA RY S Y N D RO M E
( ACS )

CHRISTIAN YOSAPUTRA, MD
RESIDEN BAGIAN ILMU PENYAKIT JANTUNG DAN PEMBULUH DARAH
FK UNSRAT / RSUP PROF. DR. RD KANDOU. MANADO
U P D AT E F R O M G U I D E L I N E S
 PEDOMAN TATALAKSANA
SINDROM KORONER AKUT
Disusun oleh:
PERHIMPUNAN DOKTER
SPESIALIS KARDIOVASKULAR
INDONESIA
2015

EDISI KETIGA

European Heart Journal (2016) 37, 267–315 ESC GUIDELINES European Heart Journal (2017) 00, 1–66 ESC GUIDELINES
doi:10.1093/eurheartj/ehv320 doi:10.1093/eurheartj/ehx393

2015 ESC Guidelines for the management 2017 ESC Guidelines for the management of
of acute coronary syndromes in patients
acute myocardial infarction in patients
presenting without persistent ST-segment
elevation
presenting with ST-segment elevation
Task Force for the Management of Acute Coronary Syndromes
The Task Force for the management of acute myocardial infarction
in Patients Presenting without Persistent ST-Segment Elevation in patients presenting with ST-segment elevation of the European
of the European Society of Cardiology (ESC) Society of Cardiology (ESC)
Downloaded from http://eurheartj.oxfordjournals.org/ by guest on June 15, 2016

Authors/Task Force Members: Marco Roffi* (Chairperson) (Switzerland), Authors/Task Force Members: Borja Ibanez* (Chairperson) (Spain), Stefan James*
Carlo Patrono* (Co-Chairperson) (Italy), Jean-Philippe Collet† (France), (Chairperson) (Sweden), Stefan Agewall (Norway), Manuel J. Antunes (Portugal),
Christian Mueller† (Switzerland), Marco Valgimigli† (The Netherlands),
Chiara Bucciarelli-Ducci (UK), Héctor Bueno (Spain), Alida L. P. Caforio (Italy),
Felicita Andreotti (Italy), Jeroen J. Bax (The Netherlands), Michael A. Borger
Filippo Crea (Italy), John A. Goudevenos (Greece), Sigrun Halvorsen (Norway),
(Germany), Carlos Brotons (Spain), Derek P. Chew (Australia), Baris Gencer
(Switzerland), Gerd Hasenfuss (Germany), Keld Kjeldsen (Denmark), Gerhard Hindricks (Germany), Adnan Kastrati (Germany), Mattie J. Lenzen
Patrizio Lancellotti (Belgium), Ulf Landmesser (Germany), Julinda Mehilli (Germany), (The Netherlands), Eva Prescott (Denmark), Marco Roffi (Switzerland),
Debabrata Mukherjee (USA), Robert F. Storey (UK), and Stephan Windecker Marco Valgimigli (Switzerland), Christoph Varenhorst (Sweden), Pascal Vranckx
(Switzerland) (Belgium), Petr Widimsk! y (Czech Republic)
Document Reviewers: Helmut Baumgartner (CPG Review Coordinator) (Germany), Oliver Gaemperli (CPG Review Document Reviewers: Jean-Philippe Collet (CPG Review Coordinator) (France),
Coordinator) (Switzerland), Stephan Achenbach (Germany), Stefan Agewall (Norway), Lina Badimon (Spain), Steen Dalby Kristensen (CPG Review Coordinator) (Denmark), Victor Aboyans (France),
Colin Baigent (UK), Héctor Bueno (Spain), Raffaele Bugiardini (Italy), Scipione Carerj (Italy), Filip Casselman
(Belgium), Thomas Cuisset (France), Çetin Erol (Turkey), Donna Fitzsimons (UK), Martin Halle (Germany),

* Corresponding authors: Marco Roffi, Division of Cardiology, University Hospital, Rue Gabrielle Perret-Gentil 4, 1211 Geneva 14, Switzerland, Tel: +41 22 37 23 743, Fax: +41 22 37
27 229, E-mail: Marco.Roffi@hcuge.ch
ACS
HOW TO
DIAGNOSIS ?
S I N D R O M K O R O N E R A K U T ( S K A ) M E R U PA K A N S U AT U M A S A L A H
K A R D I O V A S K U L A R YA N G U TA M A K A R E N A M E N Y E B A B K A N
A N G K A P E R A W ATA N R U M A H S A K I T D A N A N G K A K E M AT I A N
YA N G T I N G G I .

S E B A G I A N B E S A R S K A A D A L A H M A N I F E S TA S I A K U T D A R I P L A K
AT E R O M A P E M B U L U H D A R A H K O R O N E R YA N G K O YA K ATA U
P E C A H . I N FA R K M I O K A R D T I D A K S E L A L U D I S E B A B K A N O L E H
O K L U S I T O TA L P E M B U L U H D A R A H K O R O N E R . O B S T R U K S I
S U B T O TA L YA N G D I S E R TA I V A S O K O N S T R I K S I YA N G D I N A M I S
D A PAT M E N Y E B A B K A N T E R J A D I N YA I S K E M I A D A N N E K R O S I S
JARINGAN OTOT JANTUNG (MIOKARD).
 PATHOPHYSIOLOGY OF STABLE
ANGINA AND ACS
Pathophysiology ACS

Decreased O2 Supply
•Flow- limiting stenosis

Asymptomatic
•Anemia

Myocardial Infarction
•Plaque rupture/clot

Increased O2 Demand

Angina
O2 supply/demand mismatch→Ischemia

Myocardial ischemia→necrosis
 NEW CLINICAL CLASSIFICATION OF MI

Classification Description

1 Spontaneous MI due to coronary event, i.e. plaque erosion

and/or rupture, fissuring, or dissection

2 MI secondary to ischemia due to an imbalance of O2 supply

and demand, as from coronary spasm or embolism, anemia,
arrhythmias, hypertension, or hypotension

3 Sudden unexpected cardiac death, including cardiac arrest,

with new ST-segment elevation; new LBBB; or pathologic or
angiographic evidence of fresh coronary thrombus--in the
absence of reliable biomarker findings

4a MI associated with PCI

4b MI associated with documented in-stent thrombosis

5 MI associated with CABG surgery

 WHO CRITERIA FOR AMI
A patient is diagnosed with myocardial infarction if two (probable) or
three (definite) of the following criteria are satisfied

1. Clinical history of ischemic type

of chest pain lasting for more than
20 minutes.

▪ Pressure, squeezing, fullness or pain in center of chest that

last for several minutes
▪ Chest discomfort that spreads to jaw, neck, shoulders or
arms
▪ Chest discomfort that spreads into the back or between the
shoulders
 

Other symptoms include:
▪Dizziness
▪Lightheadedness
▪Nausea
▪Sweating
▪Shortness of breath
HEART ATTACK WARNING SIGNS

• Chest discomfort
• Pressure
• Squeezing
• Fullness
• Pain
• Discomfort in other areas of the upper body
• Arms
• Jaw
• Neck
• Back
• Stomach
• Shortness of Breath
• Cold sweat, nausea or lightheadedness
• **Women have atypical presentations!! Be more wary
 CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN

CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF

ANGINA

TYPE OF PAIN DULL PRESSURE/ SHARP/STABBING

CRUSHING PAIN

DURATION 2-5 MIN, <20 MIN SECONDSTO HOURS/

CONTINUOUS

ONSET GRADUAL RAPID

LOCATION/CHEST WALL SUBSTERNAL, NOT LATERAL CHEST WALL/

TENDERNESS TENDER TO PALP. TENDER TO PALP.
REPRODUCIBALITY WITH EXERTION/ACTIVITY WITH BREATHING/MOVING

AUTONOMIC SYMPTOMS PRESENT USUALLY ABSENT

 Differential Diagnosis (Chest Pain):
Other Cardiovascular and Nonischaemic

• Gastroesophageal
• Cervical disc or
reflux (GERD) and
neuropathic pain
spasm
• Biliary or pancreatic
• Chest-wall pain pain
• Pleurisy • Somatization and
• Peptic ulcer disease psychogenic pain
• Panic attack disorder
 WHO CRITERIA FOR AMI

A patient is diagnosed with myocardial infarction if two (probable) or

three (definite) of the following criteria are satisfied

2. Changes in serial ECG tracings.

ECG LEADS & LOCATION OF
MCI
dalah kandidat terapi reperfusi. Oleh karena itu pasien dengan EKG yang
agnostik untuk STEMI dapat segera mendapat terapi reperfusi sebelum has
emeriksaan marka jantung tersedia.

Tabel 2. Lokasi infark berdasarkan sadapan EKG

Sadapan dengan Deviasi Segmen ST Lokasi Iskemia atau Infark

V1-V4 Anterior
V5-V6, I, aVL Lateral
II, III, aVF Inferior
V7-V9 Posterior
V3R, V4R Ventrikel kanan

ersangkaan adanya infark miokard menjadi kuat jika gambaran EKG pasien
engan LBBB baru/persangkaan baru juga disertai dengan elevasi segmen S
 .. sons but because the pain is associated with sympathetic a
..
Table 3 Atypical electrocardiographic presentations .. which causes vasoconstriction and increases the workloa
that should prompt a primary percutaneous coronary .. heart. Titrated intravenous (i.v.) opioids (e.g. morphine) are
..
intervention strategy in patients with ongoing symp- .. gesics most commonly used in this context. However, morp
toms consistent with myocardial ischaemia .. is associated with a slower uptake, delayed onset of act
..
.. diminished effects of oral antiplatelet agents (i.e. clopidogrel
.. lor, and prasugrel), which may lead to early treatment failur
..
. ceptible individuals.61–63

Relief of hypoxaemia and symptoms

Recommendations Classa Lev

Hypoxia

Oxygen is indicated in patients with hypo-

I C
xaemia (SaO2 < 90% or PaO2 < 60 mmHg).

Routine oxygen is not recommended in

III B
patients with SaO2 ! 90%.64–66

Symptoms

Titrated i.v. opioids should be considered to

IIa C
relieve pain.

A mild tranquillizer (usually a benzodiaze-

pine) should be considered in very anxious IIa C
patients.

ECG = electrocardiogram; LBBB = left bundle branch block; RBBB = right bundle
branch block; RV = right ventricular; STEMI = ST-segment elevation myocardial i.v. = intravenous; PaO2 = partial pressure of oxygen; SaO2 = arteria
infarction. saturation.
a
Class of recommendation.
ACUTE ANTEROSEPTAL STEMI
INFERIOR STEMI AND RV STEMI
LBBB
EXAMPLE OF ST SEGMENT
DEPRESSION

(UAP/NSTEMI)
UA - NSTEMI

T-wave inversion
 Differential Diagnosis (ECG):
Other Cardiovascular and Nonischaemic

• Pericarditis • LV hypertrophy with

• Atypical angina strain
• Early repolarization • Brugada syndrome
• Wolff-Parkinson-White • Myocarditis
syndrome • Hyperkalemia
• Deeply inverted T- • Bundle-branch blocks
waves suggestive of a • Vasospastic angina
central nervous system • Hypertrophic
lesion or apical cardiomyopathy
hypertrophic
cardiomyopathy
 WHO CRITERIA FOR AMI
A patient is diagnosed with myocardial infarction if two (probable) or
three (definite) of the following criteria are satisfied

3. Rise and fall of

serum cardiac
biomarkers such as
creatinine kinase-
MB fraction and
troponin.
Non-MI Causes of Troponin Elevation
BERDASARKAN ANAMNESIS, PEMERIKSAAN FISIK, PEMERIKSAAN
ELEKTROKARDIOGRAM (EKG), DAN PEMERIKSAAN MARKA
JANTUNG, SPEKTRUM KLINIS SINDROM KORONER AKUT DIBAGI
MENJADI:

S STEMI

K NSTEMI

A UAP
 Differential Diagnosis ACS : Life-Threatening

Aortic dissection Tension pneumothorax

Pulmonary Boerhaave syndrome (esophageal
embolus rupture with mediastinitis)
Perforating ulcer
ACS
HOW TO
MANAGE THE
PAT I E N T ?
 ..
Isolated posterior MI. In AMI of the inferior and basal portion .. therefore48indicated in these
yang cases (Chapter 9 expands on this topic).

ACS
jam. Waktu tepat untuk terapi nitrat setelah pemberian
of the heart, often corresponding to the left circumflex territory, iso- .. vardenafil belum dapat ditentukan (Kelas III-C).
..
lated ST-segment depression ! 0.5 mm in leads V1 –V3 represents .. 4.2 Relief of pain, breathlessness, and
( beMmanaged
the dominant finding. These should O NasAa C O The
STEMI. S use ) ..
.. anxiety
Tabel 13. Jenis dan dosis nitrat untuk terapi IMA

of additional posterior chest wall leads [elevation V7 –V9 ! 0.5 mm .. Relief Nitrat
of pain is of paramount Dosis importance, not only for comfort rea-
..
MORFIN .. sonsIsosorbid dinitrate (ISDN) Sublingual 2,5–15 mg (onset 5 menit)
but because the pain is associated with sympathetic activation,

M
.. which causes vasoconstrictionOraland 15-80 mg/hari dibagi 2-3 dosis
increases the workload of the
Table 3 Atypical electrocardiographic presentations
( PA I N R E L I E F ,
that should prompt a primary percutaneous coronary
..
.. heart. Titrated intravenous (i.v.)
Intravena 1,25-5 mg/jam
opioids (e.g. morphine) are the anal-
Isosorbid 5 mononitrate Oral 2x20 mg/hari
A R TinEpatients
intervention strategy RIOD I Longoing
with AT O R )
symp- .. gesics most commonly used in this context. However, morphine use
toms consistent with myocardial ischaemia
.. Oral (slow release) 120-240 mg/hari
.. is associated
Nitroglicerin with a slower Sublingual uptake, tablet
delayed
0,3-0,6onset of action, and
mg–1,5 mg
.. diminished effects oftrinitrate)
oral antiplatelet agents (i.e. clopidogrel, ticagre-

O
.. (trinitrin, TNT, glyceryl Intravena 5-200 mcg/menit

OKSIGEN .. lor, and prasugrel), which may lead to early treatment failure in sus-
.. ceptible individuals.61–63
5.1.3 Calcium channel blockers (CCBs). Nifedipin dan amplodipin mempunyai
efek vasodilator arteri dengan sedikit atau tanpa efek pada SA Node atau
Relief of hypoxaemia and symptoms
AV Node. Sebaliknya verapamil dan diltiazem mempunyai efek terhadap SA
N I T R AT
N ( PA I N R E L I E F , 32
Recommendations
PEDOMAN TATALAKSANA SINDROM KORONER AKUT
Classa Levelb

A R T E R I O D I L AT O R ) Hypoxia

Oxygen is indicated in patients with hypo-

I C

A
ASPIRIN xaemia (SaO2 < 90% or PaO2 < 60 mmHg).

( A N T I P L AT E L E T ) Routine oxygen is not recommended in

III B
patients with SaO2 ! 90%.64–66

CLOPIDOGREL /
Symptoms

CO TICAGRELOR
( A N T I P L AT E L E T )
Titrated i.v. opioids should be considered to
relieve pain.
IIa C

A mild tranquillizer (usually a benzodiaze-

pine) should be considered in very anxious IIa C

S H I G H D O S E S TAT I N patients.

( P L A Q U E S TA B I L I Z AT I O N )
ECG = electrocardiogram; LBBB = left bundle branch block; RBBB = right bundle
branch block; RV = right ventricular; STEMI = ST-segment elevation myocardial i.v. = intravenous; PaO2 = partial pressure of oxygen; SaO2 = arterial oxygen
 TIME IS
MUSCLE

16

Table 5 Summary of important time targets

igure 3 Maximum target times according to reperfusion strategy selection in patients presenting via EMS or in a non-PCI centre. ECG = electro-
rdiogram; PCI = Percutaneous Coronary Intervention; STEMI = ST-segment elevation myocardial infarction. STEMI diagnosis is the time 0 for the
rategy clock. The decision for choosing reperfusion strategy in patients presenting via EMS (out-of-hospital setting) or in a non-PCI centre is based
n the estimated time from STEMI diagnosis to PCI-mediated reperfusion. Target times from STEMI diagnosis represent the maximum time to do
ecific interventions.
fibrinolysis is contra-indicated, direct for primary PCI strategy regardless of time to PCI.
0 min is the maximum target delay time from STEMI diagnosis to fibrinolytic bolus administration, however, it should be given as
oon as possible after STEMI diagnosis (after ruling out contra-indications).

..
 STEMI

PILIHAN REPERFUSI

PRIMARY PCI

FIBRINOLITIK
 mampu melakukan IKP (<120 menit)
PRIMARY PCI
Langkah 2: Tentukan pilihan yang lebih baik antara fibrinolisis atau strategi
( I2.2.1.
K P Langkah-langkah
) pemberian fibrinolisis pada pasien STEMI
invasif untuk kasus tersebut
Langkah 1: Nilai waktu dan risiko

Waktu sejak awitan gejala (kurang dari 12 jam atau lebih dari 12 jam
Bila dengan
pasien tanda<3 jamiskemik)
dan gejala sejak serangan dan IKP dapat dilakukan tanpa penundaan,
tidakRisiko
ada preferensi
fibrinolisis dan indikasi untuk satu strategi tertentu.
kontra fibrinolisis

Waktu yang dibutuhkan untuk pemindahan ke pusat kesehatan yang

Keadaan di mana fibrinolisis lebih baik:

mampu melakukan IKP (<120 menit)

Langkah 2: Tentukan pilihan yang lebih baik antara fibrinolisis atau strategi
FIBRIN OPasien
invasif I K datang
L I Tkasus
untuk tersebut kurang dari 3 jam setelah awitan gejala dan terdapat
halangan untuk strategi invasif
Bila pasien <3 jam sejak serangan dan IKP dapat dilakukan tanpa penundaan,
tidak ada preferensi untuk satu strategi tertentu.
Strategi invasif tidak dapat dilakukan
Keadaan di mana fibrinolisis lebih baik:
Pasien datang kurang dari 3 jam setelah awitan gejala dan terdapat BILA SUDAH
* Cath-lab sedang/tidak dapat dipakai
halangan untuk strategi invasif DIPUTUSKAN
* Kesulitan mendapatkan akses vaskular
Strategi invasif tidak dapat dilakukan
UNTUK
* Cath-lab sedang/tidak dapat dipakai
DILAKUKAN
** Tidak dapat mencapai laboratorium/pusat kesehatan yang F I Bmampu
Kesulitan mendapatkan akses vaskular
RINOLITIK,
* Tidak dapat mencapai laboratorium/pusat kesehatan yang mampu
melakukan
melakukan IKP<120
IKP dalam waktu dalam
menit waktu <120 menit
HARUS SEGERA
Halangan untuk strategi invasif DIBERIKAN DI
*Halangan untuk strategi invasif
Transportasi bermasalah IGD UNTUK
* Waktu antara Door-to-balloon dan Door-to-needle lebih dari 60 menit MEMINIMALISIR
* Transportasi bermasalah
* Waktu antar kontak medis dengan balonisasi atau door-to-balloon K E T E R L A M B ATA N
*lebihWaktu antara Door-to-balloon dan Door-to-needle lebih dari 60 menit
dari 90 menit
Keadaan di mana strategi invasif lebih baik:

Tersedianya cath-lab dengan dukungan pembedahan

* Waktu antar kontak medis dengan balonisasi atau door-to-balloon

kurang dari 90 menit

* Waktu antara Door-to-balloon dan Door-to-needle kurang dari 1 jam

Risiko tinggi STEMI

* Syok kardiogenik

* Kelas Killip ≥ 3

Indikasi kontra untuk fibrinolisis, termasuk peningkatan risiko perdarahan

dan perdarahan intrakranial

Pasien datang lebih dari 3 jam setelah awitan gejala

Diagnosis STEMI masih ragu-ragu

Tabel 20. Indikasi kontra terapi fibrinolitik

Indikasi Kontra Absolut Indikasi Kontra Relatif

Stroke hemoragik atau stroke yang
penyebabnya belum diketahui, dengan
awitan kapanpun
Stroke iskemik 6 bulan terakhir
Kerusakan sistem saraf sentral dan
neoplasma
Trauma operasi/trauma kepala yang
berat dalam 3 minggu terakhir
Transient Ischaemic Attack (TIA) dalam 6
bulan terakhir
Pemakaian antikoagulan oral
Kehamilan atau dalam 1 minggu post-
partum
Tempat tusukan yang tidak dapat
dikompresi
 Diagnosis STEMI masih ragu-ragu

Tabel 20. Indikasi kontra terapi fibrinolitik

Indikasi Kontra Absolut Indikasi Kontra Relatif

Stroke hemoragik atau stroke yang Transient Ischaemic Attack (TIA) dalam 6
penyebabnya belum diketahui, dengan bulan terakhir
awitan kapanpun
Stroke iskemik 6 bulan terakhir Pemakaian antikoagulan oral
Kerusakan sistem saraf sentral dan Kehamilan atau dalam 1 minggu post-
neoplasma partum
Trauma operasi/trauma kepala yang Tempat tusukan yang tidak dapat
berat dalam 3 minggu terakhir dikompresi
Perdarahan saluran cerna dalam 1 bulan Resusitasi traumatik
terakhir
Penyakit perdarahan Hipertensi refrakter (tekanan darah sistolik
>180 mmHg)
Diseksi aorta Penyakit hati lanjut
Infeksi endokarditis
Ulkus peptikum yang aktif

54 PEDOMAN TATALAKSANA SINDROM KORONER AKUT

 Tabel 21. Regimen fibrinolitik untuk infark miokard akut

Dosis awal Koterapi Indikasi kontra

antitrombin spesifik
Streptokinase (Sk) 1,5 juta U dalam 100 mL Heparin i.v. Sebelum Sk
Dextrose 5% atau larutan selama 24-48 atau
salin 0,9% dalam waktu 30- jam anistreplase
60 menit
Alteplase (tPA) Bolus 15 mg intravena Heparin i.v.
0,75 mg/kg selama 30 menit, selama 24-48
kemudian 0,5 mg/kg selama jam
60 menit
Dosis total tidak lebih dari
100 mg

2.3. Koterapi antikogulan

1. Pasien yang mendapat terapi reperfusi fibrinolisis, sebaiknya diberikan

terapi antikoagulan selama minimum 48 jam (Kelas II-C) dan lebih baik
selama rawat inap, hingga maksimum 8 hari (dianjurkan regimen non
UFH bila lama terapi lebih dari 48 jam karena risiko heparin-induced
thrombocytopenia dengan terapi UFH berkepanjangan (Kelas II-A)

2. Pasien STEMI yang tidak mendapat terapi reperfusi, dapat diberikan terapi
antikoagulan (regimen non-UFH) selama rawat inap, hingga maksimum 8
GUIDELINES STEMI
ESC 2017

1
Figure 5 “Do not forget” interventions in STEMI patients undergoing a primary PCI strategy. ACE = angiotensin-converting enzyme; DAPT = dual
antiplatelet therapy; DES = drug eluting stent; ECG = electrocardiogram; echo = echocardiogram; ED = emergency department; HF = heart failure;
i.v. = intravenous; IRA = infarct related artery; LVEF = left ventricular ejection fraction; MRA = mineralcorticoid receptor antagonist; PCI = percuta-
Figure 6 “Do not forget” interventions in STEMI patients undergoing a successful fibrinolysis strategy. ACE = angiotensin-converting enzyme;
DAPT = dual antiplatelet therapy; DES = drug eluting stent; ECG = electrocardiogram; echo = echocardiogram; HF = heart failure; i.v. = intravenous;
 MINOCA
44 ESC Guidelines

( M Y O C A R D I A L I N FA R C T I O N I N N O N O B S T R U C T I V E CORONARY ARTERY )
 Low Likelihood
Likelihoo
od High Likelihood
Likelihoo

1. Presentation

2. ECG

3. Troponin

4. Diagnosis Non-cardiac UA Other NSTEMI STEMI

Cardiac

STEMI = ST-elevation myocardial infarction; NSTEMI = non-ST-elevation myocardial infarction; UA = unstable angina.

Figure 1 Initial assessment of patients with suspected acute coronary syndromes. The initial assessment is based on the integration of low-
likelihood and/or high-likelihood features derived from clinical presentation (i.e., symptoms, vital signs), 12-lead ECG, and cardiac troponin. The pro-
portion of the final diagnoses derived from the integration of these parameters is visualized by the size of the respective boxes. “Other cardiac”

UAP / NSTEMI
includes, among other, myocarditis, Tako-Tsubo cardiomyopathy, or tachyarrhythmias. “Non-cardiac” refers to thoracic diseases such as pneumonia
or pneumothorax. Cardiac troponin should be interpreted as a quantitative marker: the higher the level, the higher the likelihood for the presence of
myocardial infarction. In patients presenting with cardiac arrest or haemodynamic instability of presumed cardiovascular origin, echocardiography
should be performed/interpreted by trained physicians immediately following a 12-lead ECG. If the initial evaluation suggests aortic dissection or
 PERIKSA ENZIM JANTUNG
UAP / NSTEMI
276
( TROPONIN )
ESC Guidelines

Acute Chest Pain

hs-cTn
hs-cTn<ULN
<ULN hs-cTn
hs-cTn>ULN
>ULN

Pain
Pain>6h
>6h Pain
Pain<6h
<6h

Re-test hs-cTn: 3h

Highly abnormal hs-cTn

+ clinical presentation
hs-cTn
hs-cTnno
nochange
change changeaa
∆∆ change
hs-cTn
hs-cTnno
nochange
change
(1(1 value
value >>ULN)
ULN)

Painfree,
Painfree,GRACE
GRACE<140,
<140,
Work-up
Work-updifferential
differential
differential
differentialdiagnoses
diagnosesexcluded
excluded
diagnoses
diagnoses

Discharge/Stresstesting
Discharge/Stress testing Invasivemanagement
Invasive management

GRACE = Global Registry of Acute Coronary Events score; hs-cTn = high sensitivity cardiac troponin; ULN = upper limit of normal, 99th percentile of healthy controls.
a

Figure 2 0 h/3 h rule-out algorithm of non-ST-elevation acute coronary syndromes using high-sensitivity cardiac troponin assays.
 only CK-MB and
symptoms and with
copeptin seem
normal to have
ECG do not necessarily require rhythm

als.org/ by guest on June 15, 2016

4 – 50
CK-MB shows
monitoring a moreadmission.
or hospital rapid decline Suspected NSTEMI
h cardiac
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patients at provide
low risk added
for cardiac arrhythmias require
yocardial injury and the detection of early
rhythm monitoring for ≤24 h or until coronary revascularization 0h B ng/l 0h D ng/l
ment of copeptin, the C-terminal part of 0h <A*ng/l or and Other or
(whichever comes first) in an intermediate or coronary care unit,
0-1h C ng/l 0-1h E ng/l
one, may quantify the endogenous stress
while individuals
onditions at intermediate
including MI. As the level ofto
en-high risk for cardiac arrhythmia
omay requirehigh
be invariably rhythm monitoring
at the onset of MI, thefor .24 h in an intensiveRule-out
or
Observe Rule-in
coronary
to care unit
conventional (less or in an intermediate
sensitive) cardiac care unit, depending on
the 44clinical
ntial. – 50
presentation,
Therefore degree
the routine use ofof revascularization and early A B C D E
l post-revascularization
biomarker for the earlycourserule-out of MI7). It is recommended
(Table that per- 5
hs-cTnT (Elecsys) 12 3 52 5
ver sensitive
sonnel or high-sensitivity
adequately equipped and cardiac
trained to manage hs-cTnl (Architect)
life-threatening 2 5 2 52 6
hs-cTnl (Dimension Vista)+ 0.5 5 2 107 19
vailable. Copeptin may have some added
sitivity cardiac troponin in the early rule-
Table 7 Recommended unit and duration of cardiac
Figure 3 0 h/1 h rule-in and rule-out algorithms using high-
rhythm monitoring according to clinical presentation
sensitivity cardiac troponins (hs-cTn) assays in patients presenting
afteralgorithms
e-out’ established NSTE-ACS diagnosiswith suspected non-ST-elevation myocardial infarction (NSTEMI)
vity and diagnostic accuracy for the detec- to the emergency department. 0 h and 1 h refer to the time from
first blood test. NSTEMI can be ruled-out already at presentation,
Rhythm
tation, theClinical
time Presentation
interval to the second car- Unit
monitoring
if the hs-cTn concentration is very low. NSTEMI can also be ruled-
nt can be shortened with the use of
Unstable angina Regular ward or discharge out by theNone
combination of low baseline levels and the lack of a rele-
his may reduce substantially the delay to
NSTEMI at low risk for cardiac Intermediate care unit vant increase within 1 h. Patients have a high likelihood for NSTEMI
o shorter stays ain the emergency depart- ≤24 h
arrhythmias or coronary care unit if the hs-cTn concentration at presentation is at least moderately
,8,10,29 – 36
NSTEMIIt isat intermediate
recommended to use the care units elevated
to high Intensive/coronary or or hs-cTn concentrations show a clear rise within the first
>24 h
2). As an alternative,
risk for 0 h/1
cardiac arrhythmias b
h assessments
intermediate care unit hour. Cut-off levels are assay-specific. Cut-off levels for other
high-sensitivity cardiac troponin assays hs-cTn assays are in development. *Only applicable if chest pain
 STRATIFIKASI RISIKO
296 NSTEMI ESC Guidelines
( TIMI SCORE , GRACE SCORE )

Symptoms Onset

First medical contact NSTE-ACS diagnosis

PCI center EMS or Non–PCI center

Immediate transfer to PCI center

Very high Very high
Risk stratification

Same-day transfer
High High

Transfer

Downloaded from http://eurheartj.oxfordjournals.org/ by gu

Intermediate Intermediate

Transfer
optional
Low Low
Therapeutic
strategy

Immediate Early Non-invasive

Invasive
Invasive invasive testing if
(<72 hr)
(<2 hr) (<24 hr) appropriate

EMS = emergency medical services; PCI = percutaneous coronary intervention.

 TIMI telah divalidasi untuk prediksi kematian 30 hari dan 1 tahun pada berbagai
S T R A T I Fspektrum
IKASI R SKA
I S termasuk
IKO —> UAP/NSTEMI.
TIMI SCORE

Tabel 4. Skor TIMI untuk UAP dan NSTEMI

Parameter
Usia > 65 tahun 1
Lebih dari 3 faktor risiko* 1
Angiogram koroner sebelumnya menunjukkan stenosis >50% 1
Penggunaan aspirin dalam 7 hari terakhir 1
Setidaknya 2 episode nyeri saat istirahat dalam 24 jam terakhir 1
Deviasi ST > 1 mm saat tiba 1
Peningkatan marka jantung (CK, Troponin) 1

*Faktor risiko: hipertensi, DM, merokok, riwayat dalam keluarga, dislipidemia

Tabel 5. Stratifikasi risiko berdasarkan skor TIMI

Skor TIMI Risiko Risiko Kejadian Kedua

0-2 Rendah <8,3 %
3-4 Menengah <19,9%
5-7 Tinggi ≤41%
 ≤88 dianggap mempunyai risiko rendah (risiko kematian <3%). Sementara itu,
pasien dengan skor risiko GRACE 89-118 dan >118 berturutan mempunyai
STRATIFIKASI RISIKO —> GRACE SCORE
risiko kematian menengah (3-8%) dan tinggi (>8%).

Tabel 6. Skor GRACE

Prediktor Skor 140-159 26

Usia dalam tahun 160-199 11
<40 0 >200 0
40-49 18 Kreatinin (µmol/L)
50-59 36 0-34 2
60-69 55 35-70 5
70-79 73 71-105 8
80 91 106-140 11
Laju denyut jantung (kali per menit) 141-176 14
<70 0 177-353 23
70-89 7
≥354 31
90-109 13
Gagal jantung berdasarkan klasifikasi Killip
110-149 23
I 0
150-199 36
II 21
>200 46
III 43
Tekanan darah sistolik (mmHg)
IV 64
<80 63
Henti jantung saat tiba di RS 43
80-99 58
Peningkatan marka jantung 15
100-119 47
Deviasi segmen ST 30
120-139 37

Stratifikasi risiko berdasarkan kelas Killip merupakan klasifikasi risiko

PEDOMAN TATALAKSANA SINDROM KORONER AKUT 23
berdasarkan indikator klinis gagal jantung sebagai komplikasi infark miokard
akut dan ditujukan untuk memperkirakan tingkat mortalitas dalam 30 hari
(Tabel 7). Klasifikasi Killip juga digunakan sebagai salah satu variabel dalam
GRACE SCORE : klasifikasi GRACE.

> 140 : HIGH RISK

> 1 0 9 ATA U < 1 4 0 : I N T E R M E D I AT E R I S K
< 109 : LOW RISK
 coronary syndromes In ESC Guidelines
In patients
patients with
with multivessel
multivessel CAD,

djournals.org/
rdjournals.org/by
CAD,
itit is recommended to base
is recommended to base the the
a b c revascularization
revascularization strategy
strategy (e.g.
(e.g. ad
ad
Recommendations
Recommendations Class
Classa Level
Levelb Ref.
Ref.c hoc culprit-lesion PCI, multivessel
hoc culprit-lesion PCI, multivessel
be discussed
An within the Heart Team if delayed CABG of
An immediate
immediate invasive
invasive strategy
strategy PCI,
An PCI, CABG)
invasive on
on the
CABG)strategythe clinical
(<72status
clinical h) is
status
ulprit (<2
vessels
h)
h) is is an option.
is recommended in
in patients
patients with II C

byguest
(<2 recommended with and comorbidities as well as the C
recommended in patients withthe
and comorbidities as well as at least
at least one of the following

gueston
at least one of the following disease
disease severity
severity (including
(including
very-high-risk criteria: onedistribution,
of the following intermediate-risk
very-high-risk
nagement criteria:
of patients with cardiogenic shock distribution, angiographic
angiographic lesion
lesion
criteria:

onJune
–– haemodynamic
haemodynamic instability
instability or
or characteristics, SYNTAX
characteristics, SYNTAX score), score),
nic shock may develop in up to 3% of NSTE-ACS patients diabetesto
tomellitus

June15,
cardiogenic shock –according the
cardiogenic shock according the local
local Heart
Heart Team
Team
spitalization and has
–– recurrent
recurrent or become
or ongoing
ongoing the most frequent cause of
chest
chest renal
–protocol.
protocol. insufficiency (eGFR

15,2016
pain refractory to 2
pain
l mortalitytreatment refractory
in this setting.to medical
382 – 384
medical One orI moreCpartial or In ,60 mL/min/1.73 m)
In patients
patients in
in whom
whom aa short
short DAPT
DAPT

2016
treatment I C LVEF
–duration ,40% or congestive
duration (30 days) is planned because
(30 days) is planned heart
because
322,
vessel occlusions may
–– life-threatening result
arrhythmias
life-threatening arrhythmias orin severe
or heart failure, espe- I A
cardiac of failure
of an
an increased
increased bleeding
bleeding risk,
risk, aa new-
new- IIb
IIb B
B 245324
245
cardiac arrest
ses of pre-existing LV dysfunction, reduced cardiac output
arrest early
–generation post-infarction
DES may be angina
considered
–– mechanical generation DES may be considered
mechanical complications
complications of of MI
MI
ctive peripheral
–– acute
organ perfusion. More than two-thirds of –over
over aa BMS.
recent PCI
BMS.
acute heart
heart failure
failure with
with refractory
refractory
ave three-vessel
angina
angina or CAD.
or ST Cardiogenic shock may also be re-
ST deviation
deviation
– prior CABG
– recurrent dynamic ST- – GRACE riskstent;
score .109 and artery
mechanical complications of or T-wave including mitral re-
NSTEMI, BMS
BMS ¼ bare-metal
¼ bare-metal stent; CABG
CABG ¼ coronary
¼ coronary artery bypass
bypass grafting;
grafting;
changes, particularly with CAD
CAD ¼ coronary artery disease; DAPT ¼ dual (oral) antiplatelet therapy;
¼ coronary
,140, artery disease; DAPT ¼ dual (oral) antiplatelet therapy;
n related tointermittent
papillaryST-elevation.
muscle dysfunction or rupture and DES ¼ drug-eluting stent;
or recurrent symptoms or known
DES ¼ drug-eluting stent; eGFR
eGFR ¼
¼ estimated
estimated glomerular
glomerular filtration
filtration rate;
rate;
r septal or free wall rupture. In patients with cardiogenic GRACE ¼ Global Registry of Acute Coronary Events; LVEF ¼ left ventricular
An early invasive strategy (<24 h) ischaemia on non-invasive testing.
ejection fraction; MI ¼ myocardial infarction; NSTE-ACS ¼ non-ST-elevation
ejection fraction; MI ¼ myocardial infarction; NSTE-ACS ¼ non-ST-elevation
mediate coronary angiography
is recommended in patients withisatindicated and PCI is the acute coronary syndromes; PCI ¼ percutaneous coronary intervention;
In patients with none of the above
uentlyleast one revascularization
used of the following high-risk
modality. If the coronary SYNTAX ¼ SYNergy between percutaneous coronary intervention with
mentioned risk criteria
criteria: 303, TAXus and cardiac surgery.and no
s not suitable for PCI, patients should
– rise or fall in cardiac troponin
undergo
I A
emergent
326, recurrent symptoms,
Timing to coronary non-invasive
angiography is calculated from hospital admission.
aa 113,
he value ofcompatible
intra-aortic balloon counterpulsation in327
with MI MI testing
Class for ischaemia
of recommendation.(preferably I A
bbLevel of evidence. 114

Downloaded from http://eurheartj.oxfordjournals.org/ by guest o

– dynamic ST-
ed by cardiogenic or T-wave
shock has changes 385
been challenged. Extra- with
cc imaging) is recommended
References supporting level of evidence.
(symptomatic or silent) before deciding on an invasive
l membrane – GRACEoxygenation
score .140. and/or implantable LV assist evaluation.
ay be considered in selected patients.
In centres experienced with radial
commendations for invasive coronary access, a radial approach is
I A 251
phy and revascularization in non-ST-elevation recommended for coronary
angiography and PCI.
ronary syndromes
In patients undergoing PCI, 242,
new-generation DESs are 252,
mmendations for invasive coronary angiography I A
recommended. 386–
vascularization in non-ST-elevation acute 390
ary syndromes
In patients with multivessel CAD,
it is recommended to base the
revascularization strategy (e.g. ad
mmendations Classa Levelb Ref.c
hoc culprit-lesion PCI, multivessel
mediate invasive strategy PCI, CABG) on the clinical status
is recommended in patients with and comorbidities as well as the I C
one of the following disease severity (including
gh-risk criteria: distribution, angiographic lesion
 penyekat
CABG), beta
perlu yang sering dipakai
dipertimbangkan dalam praktek
penundaan klinik dapat
pembedahan dilihat5pada
selama hari
sebaiknya mendapat nitrat sublingual setiap 5 menit sampai maksimal kiri ≤40% dan pasien dengan diabetes mellitus, hipertensi, atau penyakit
tabel 12.
setelah penghentian pemberian ticagrelor atau clopidogrel bila secara
3 kali pemberian, setelah itu harus dipertimbangkan penggunaan ginjal kronik (PGK) (Kelas I-A).
Tabel 12. Jenis dan
klinis memungkinkan, dosisbila
kecuali penyekat betarisiko
terdapat untuk terapi
kejadianIMAiskemik yang Tabel 16. Jenis dan dosis antikoagulan untuk IMA
nitrat intravena jika tidak ada indikasi kontra (Kelas I-C).
tinggi (Kelas IIa-C). 2. Inhibitor ACE hendaknya dipertimbangkan pada semua penderita selain
Penyekat beta Selektivitas Aktivitas agonis parsial Dosis untuk angina
3. Nitrat intravena diindikasikan pada iskemia yang persisten, gagal Antikoagulan Dosis
10. Atenolol
Ticagrelor atau B1clopidogrel perlu dipertimbangkan
-
jantung, atau hipertensi dalam 48 jam pertama UAP/NSTEMI.
untuk
50-200diberikan seperti di atas (Kelas IIa-B). Pilih jenis dan dosis inhibitor ACE yang telah
mg/hari (atau
Bisoprolol B1 - 10 mg/hari
Fondaparinuks 2,5 mg subkutan
dilanjutkan) setelah pembedahan CABG begitu dianggap aman (Kelas
Keputusanamenggunakan
Carvedilol dan b nitrat+intravena tidak 2x6,25
bolehmg/hari, direkomendasikan
menghalangi Enoksaparin berdasarkan kali sehari yang ada (Kelas IIa-C).
1mg/kg, duapenelitian
IIa-B).
pengobatan yang terbukti menurunkan mortalitas seperti
titrasi sampaipenyekat Heparin tidak Bolus i.v. 60 U/g, dosis
3. Penghambat reseptor angiotensin diindikasikan bagi pasien infark
11. Tidakbeta
disarankan memberikan
atau angiotensin aspirin enzymes
converting bersama inhibitor
NSAID (penghambat 2x25 COX-
(ACE-I) (Kelas
maksimum I-B). terfraksi maksimal 4000 U.
2 selektif dan NSAID non-selektif ) (Kelas III-C). mg/hari mikoard yang intoleran terhadap inhibitor ACE dan mempunyai fraks
4. Nitrat tidak diberikan pada pasien dengan tekanan darah sistolik Infus i.v. 12 U/kg selama
Metoprolol B1 - 50-200 mg/hari
Keterangan:
<90DAPT
mmHg perlu tetap
atau >30 diberikan
mmHg selama 12 bulan
di- bawah tanpa
nilai awal, memperdulikan
bradikardia
ejeksi ventrikel kiri ≤40%,
24-48dengan
jam dengan atau tanpa
dosis gejala
maksimal 1000klinis
U/jamgagal jantung
Propanolol Nonselektif 2x20-80 mg/hari berat
jenis stent.(<50 kali permenit), takikardia tanpa gejala gagal jantung, atau infark(Kelas I-B). target aPTT 1½-2x kontrol
ventrikel kanan (Kelas III-C).
Tabel 10. Jenis dan dosis antiplatelet untuk terapi IMA
5.1.2 Nitrat. Keuntungan terapi nitrat terletak pada efek dilatasi vena Tabel 17. Jenis dan dosis inhibitor ACE untuk IMA
5. Nitrat tidak boleh diberikan pada pasien yang telah mengkonsumsi 5.5. Kombinasi Antiplatelet dan Antikoagulan
Antiplatelet Dosis
yang mengakibatkan berkurangnya preload dan volume akhir diastolik
inhibitor fosfodiesterase: sidenafil dalam 24 jam, tadalafil dalam Inhibitor ACE dosis
Aspirin Dosis
ventrikel kiri loading 150-300
sehingga mg, dosis
konsumsi pemeliharaan
oksigen 75-100berkurang.
miokardium mg Efek
48 jam. Waktu yang tepat untuk terapi nitrat setelah 1. Penggunaan
pemberian warfarin bersama aspirin dan/atau clopidogrel meningkatkan
Ticagrelor Dosis loading 180 mg, dosis pemeliharaan 2x90 mg/hari
lain dari nitrat adalah dilatasi pembuluh darah koroner baik yang normal Captopril 2-3 x 6,25-50 mg
vardenafil
Clopidogrel Dosisbelum
loadingdapat ditentukan
300 mg, (Kelas III-C).
dosis pemeliharaan 75 mg/hari risiko perdarahan dan oleh karena itu harus dipantau ketat (Kelas I-A).
maupun yang mengalami aterosklerosis. Ramipril 2,5-10 mg/hari dalam 1 atau 2 dosis

Tabel 13.intravena
Jenis dan dosis nitrat untuk terapi IMA 2. Kombinasi aspirin, clopidogrel
Lisinopril dan dalam
2,5-20 mg/hari antagonis
1 dosisvitamin K jika terdapat
1. Nitrat oral atau efektif menghilangkan keluhan dalam fase
5.3. Penghambat Reseptor Glikoprotein IIb/IIIa Enalapril 5-20 mg/hari dalamdalam
1 atau 2waktu
dosis sesingkat mungkin
Nitrat akut dari episode anginaDosis (Kelas I-C). indikasi dapat diberikan bersama-sama
Pemilihan
Isosorbid kombinasi agen antiplatelet
dinitrate (ISDN) Sublingualoral, agen
2,5–15 penghambat
mg (onset 5 menit) reseptor
dan dipilih targen INR terendah yang masih efektif. (Kelas IIa-C).
2. Pasien dengan UAP/NSTEMI yang mengalami nyeri dada berlanjut
glikoprotein IIb/IIIa dan antikoagulan dibuat
Oral 15-80 berdasarkan
mg/hari risiko kejadian
dibagi 2-3 dosis
I-C). Penggunaan
iskemik dan perdarahan (Kelas Intravena 3. Jika antikoagulan diberikan bersama aspirin dan clopidogrel, terutama
1,25-5 mg/jampenghambat reseptor
5.7. Statin
PEDOMAN TATALAKSANA SINDROM KORONER AKUT 31
Isosorbid 5 IIb/IIIa
glikoprotein mononitrate Oral
dapat diberikan 2x20pasien
pada pada penderita tua atau yang risiko tinggi perdarahan, target INR 2- 2,5
mg/hariIKP yang telah mendapatkan
Oral (slow release) 120-240 mg/hari
Tanpa melihat nilai awal kolesterol LDL dan tanpa mempertimbangkan
DAPT dengan risiko tinggi (misalnya peningkatan troponin, trombus yang
lebih terpilih (Kelas IIb-B).
Nitroglicerin Sublingual tablet 0,3-0,6 mg–1,5 mg
terlihat) apabila risiko perdarahan rendah (Kelas I-B). Agen ini tidak disarankan
modifikasi diet, inhibitor hydroxymethylglutary-coenzyme A reductase (statin)
(trinitrin, TNT, glyceryl trinitrate) Intravena 5-200 mcg/menit
diberikan secara rutin sebelum angiografi (Kelas III-A) atau pada pasien yang
harus diberikan pada semua penderita UAP/NSTEMI, termasuk mereka yang
5.6. Inhibitor
telah menjalaniACE danrevaskularisasi,
terapi Penghambat Reseptor Angiotensin
jika tidak terdapat indikasi kontra (Kelas
5.1.3 Calcium channel blockers (CCBs). Nifedipin dan amplodipin mempunyai
PEDOMAN TATALAKSANA SINDROM KORONER AKUT 35
efek vasodilator arteri dengan sedikit atau tanpa efek pada SA Node
I-A). atau
Terapiangiotensin
Inhibitor statin dosisconverting
tinggi hendaknya
enzyme dimulai sebelumdalam
(ACE) berguna pasienmengurangi
keluar rumah
AV Node. Sebaliknya verapamil dan diltiazem mempunyai efek terhadap SA
remodeling
sakit, dengandan menurunkan
sasaran angkamencapai
terapi untuk kematian penderita pascainfark-miokard
kadar kolesterol LDL <100 mg/
 5.9.3 Recommendations for long-term management after

ttp://eurheartj.oxfordjournals.org/ by guest on June 15, 2016

non-ST-elevation acute coronary syndromes Variations in the application of evidence-based strategies are associated
with significant differences in outcome. Several large registries have
the CV disease, the older the patient, the longer the diabetes dur- shown deficiencies in the treatment of NSTE-ACS patients when com-
Recommendations for long-term management after Participation in a well-structured cardiac
ation and the more comorbidities that are present, the less stringent pared with recommendations from contemporary guidelines. 535, Under-
non-ST-elevation acute coronary syndromes rehabilitation programme to modify
the glucose control should be. utilization of evidence-based treatments IIa is common.
A 541–
Adherence to
lifestyle habits and increase adherence
546
Core components and goals of cardiac rehabilitation, including toguidelines
treatmenthas been
should becorrelated
considered.with improvements in patient outcomes
Recommendations
physical activity counselling, diet/nutrition
(for the Classa smoking
counselling, Levelb ces-
Ref.c in ACS, including reduced mortality.550,551 Thus priority needs to be gi-
In patients with LDL cholesterol
recommendations
sation, weight on antithrombotic
control and goals for lipid and blood pressure man- ≥70venmg/dL
to improving the utilization
(≥1.8 mmol/L) despite of
a evidence-based guidelines. Continu-
treatment, see sections 5.2.9 and 5.3.3) ous monitoring
agement should be stated in the discharge letter.534 maximally toleratedof performance
statin indicators
dose, further IIa is strongly
B encouraged
529 to
It is recommended to advise all enhanceinthe
reduction LDLquality of treatment
cholesterol with a and minimize unwarranted variations
e
patients
5.9.2 Lifestyle on lifestyle
changes andchanges (including
cardiac rehabilitation 536, non-statin agent should
in evidence-based be considered.
care. Consistent application of therapies based on
I A
smoking cessation, regular physical 537
Enrolment in a well-structured cardiac rehabilitation/secondary pre- A systolic blood pressure goal 547–
activity and a healthy diet). IIa B
vention programme after NSTE-ACS should be considered, as it can of ,140
Table mmHg
14 should be considered.
Performance 549
measures in NSTE-ACS
It is recommended to start
enhance patient compliance with the medical regimen and promote
high-intensity statin therapy as early as
522, patients
lifestyle changes, including
possible, regular physicaland
unless contraindicated, exerciseI and smoking
A 527,
ces- ACE ¼ angiotensin-converting enzyme; ARB ¼ angiotensin receptor blocker;
528 LDL ¼ low-density
sation, and allows
maintainforitdietary counselling.521,535 Aerobic exercise train-
long term. • Use of lipoprotein;
aspirin LVEF ¼ left ventricular ejection fraction;
NSTE-ACS ¼ non-ST-elevation acute coronary syndromes.
ing within a An cardiac rehabilitation
ACE inhibitor programme
is recommended in should be offered to a • Use of ticagrelor/prasugrel/clopidogrel
Class of recommendation.
patients afterpatients
NSTE-ACS, with≤40%
with LVEF the need for an evaluation of both478–
or heart ex- b
Level of evidence.
• Use of fondaparinux/bivalirudin/UFH/enoxaparin
481, c
References supporting level of evidence.
ercise capacityfailure,
and hypertension or diabetes,
exercise-associated risk. If feasible,
I regularA exercise
530, d • Use of,221
Serum creatinine beta-blocker
mmol/Lat(2.5discharge
mg/dL)infor
patients
men andwith,177
LV dysfunction
mmol/L
unless contraindicated. An ARB
training three or more times a week and 30 min per session is recom- 531, (2.0 mg/dL)• for
Usewomen; serum potassium concentration ,5.0 mmol/L.
of statins
provides an alternative, particularly if

Downloaded from http://eurheartj.oxfordjournals.org/ by

mended. Sedentary patients 538
are should be strongly encouraged to start e
At the time of finalizing the guidelines, this recommendation applies only to ezetimibe.
ACE inhibitors not tolerated. • Use of ACE-inhibitor or ARB in patients with systolic LV dysfunction
light-intensity exercise programmes after adequate exercise-related or heart failure, hypertension or diabetes
Beta-blocker therapy is recommended
risk stratification. Smoking
in patients with cessation
LVEF ≤40%, is aunless
highly effective
I measureA to482–
re- • Use of early invasive procedures in intermediate- to high-risk patients
duce morbidity and mortality in patients after ACS. 521,536 486
contraindicated.
Mineralocorticoid receptor
6. Performance measures
• Smoking cessation advice/counselling

5.9.3 Recommendations foreplerenone,

long-term • Enrolment in a secondary prevention/ cardiac rehabilitation
antagonists, preferably are management after Variations in the application of evidence-based strategies are associated
programme
non-ST-elevation acute
recommended coronary
in patients with syndromes
LVEF 487,
≤35% and either heart failure or I A 488,
with significant differences
• Development in outcome.
of regional Severalprogrammes
and/or national large registries
to measurehave
performance
shown deficiencies in theindicators
treatmentsystematically
of NSTE-ACS and patients
provide feedback
when com- to
diabetes after NSTE-ACS but no
Recommendations for long-term management after 525 individual hospitals
significant renal dysfunction or pared with recommendations from contemporary guidelines. Under-
non-ST-elevation
hyperkalaemia.acute
d coronary syndromes
utilization of evidence-based treatments is common. Adherence to
ACE ¼ angiotensin-converting enzyme; ARB ¼ angiotensin receptor blocker;
A diastolic blood pressure goal of ,90
539,
guidelines has been correlated with improvements in patient outcomes
LV ¼ left ventricular; NSTEMI ¼ non-ST-elevation myocardial infarction;
mmHg is recommended (,85 mmHg a I A c in ACS, UFH
including mortality.550,551 Thus priority needs to be gi-
reduced heparin.
Recommendations (for the Class Levelb Ref. 540 ¼ unfractionated
in diabetic patients).
recommendations on antithrombotic ven to improving the utilization of evidence-based guidelines. Continu-
treatment, see sections 5.2.9 and 5.3.3) ous monitoring of performance indicators is strongly encouraged to
TERIMA KASIH